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3. Food Animal 3 > Lymphoid system > Flashcards

Lymphoid system Flashcards

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1
Q

Caseous Lymphadenitis
- species affected
- geographic distribution

A

Species affected:
◦ Sheep & goats
◦ (Cattle, horses, alpacas, camels, buffalo)
◦ Zoonotic potential > CLA, pneumonia
*Geographical distribution: Worldwide

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2
Q

Caseous Lymphadenitis
- organism characteristics

A

◦ Corynebacterium pseudotuberculosis
◦ Gram +, diptheroid, facultative anaerobe, facultative intracellular
bacillus
<><>
2 Biotypes
◦ Nitrate negative - sheep & goats
◦ Nitrate positive - Associated with ulcerative lymphangitis in horses/cattle- more common dry
western states (California)

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3
Q

Caseous Lymphadenitis
virulence factors and toxins

A

Lipid layer outside cell wall
◦ Allows intracellular persistence, resists killing by phagocytes
<><>
Phospholipase D (PLD):
◦ Exotoxin, cytotoxic and partial hemolysin
◦ Promotes local inflammation & necrosis
◦ Damages endothelial cells
◦ Can cause lymphatic thrombosis
<><>
Other toxins:
◦ Sphingomyelinase
◦ Inhibitory factor of Staphylococcal beta-hemolysin
◦ Hemolysis factor
◦ Dermatonecrotoxins
◦ Mouse-lethality toxins

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4
Q

Caseous Lymphadenitis
- pathogenesis

A
  • Skin penetration (inhale, ingest, umbilical)
  • Immediate phagocytosis by leukocytes
  • Survival in leukocyte
  • Transportation to LN → multiplication
  • Host cell dies releasing bacteria
  • Lymphogenous & hematogenous spread
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5
Q

Caseous Lymphadenitis
◦ Transmission:

A

Contamination of wounds:
◦ Shearing wounds
◦ Sheep dip
◦ Fighting wounds (goats)
<><>
◦ Traumatized oral mucosa
<><>
◦ Aerosol > Pulmonary abscesses are the primary source of contamination
<><>
◦ All demonstrated transmission through environmental contamination

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6
Q

Caseous Lymphadenitis
◦ Environmental survival:

A

◦ Shaded areas - up to 20 weeks (shearing sheds)
◦ Soil - up to 8 months
- Brazilian study → semi-arid environment → up to 2 years
◦ On wood surfaces and bedding up to 8 weeks
◦ Commercial sheep dips - 24 hours
◦ Does not replicate outside of host

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7
Q

Caseous Lymphadenitis
- Prevalence
- age
- clinical vs subclinical cases?

A

Prevalence
◦ Increase with age:
◦ Australian unvaccinated sheep: 3.4% lambs→54% adult ewes
<><>
Many flocks affected
◦ Alberta serology- 50-94% incidence of exposure
◦ Australia 97% flocks (25% of sheep within affected flocks)
◦ 2003 study Quebec 21% culled sheep carcasses
◦ Goats more prevalent: Most Ontario goat herds
<><>
- Clinical cases sporadic (case incidence within flock)
◦ Subclinical cases common

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8
Q

Caseous Lymphadenitis
- how fast can in spread from one animal?

A

Introduction of infected animal to naive flock
> High incidence of abscesses 2-3 years later

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9
Q

Caseous Lymphadenitis
Clinical signs: (forms, goats vs sheep)

A

External form (abscessation of superficial lymph nodes) – more common
in goats
◦ Mild to no signs other than LN, unless obstructive
◦ Head/neck most common
◦ Lymph nodes: mandibular, parotid, prescapular, prefemoral
<><><><>
Internal or visceral form - more common sheep
◦ Deep lymph nodes: mediastinal, bronchial, mesenteric, lumbar
◦ Lung, spleen, liver, kidney
◦ Weight loss, anorexia, depression, fever, cough
<><><><>
◦ Abscesses lamellated in sheep, creamy/pasty goats

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10
Q

Caseous Lymphadenitis
Diagnosis:

A

◦ Clinical signs
<>
◦ CBC not reliable- walled off abscesses
<>
Serology: ELISA, AGID, SHI (synergistic hemolysis inhibition)
◦ Many tests (high sensitivity)
◦ Specificity poor (because of cross reactivity)
◦ ELISA: sensitivity 96% experimental, 81% natural infection in sheep
<>
◦ Aspiration of abscess: cytology/culture (ddx– Trueperella pyogenes, Staph. aureus, P.
multocida, anaerobes)
<>
Post-mortem:
◦ Abscesses in LN, peripheral or visceral or within lung parenchyma.
◦ Localized infection

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11
Q

Caseous Lymphadenitis
Treatment:

A

Walled off abscesses
◦ Antibiotics have not proven to be of value
◦ Sensitive to many antibiotics in vitro
> Penicillins
> Tulathromycin – subcutaneous, intralesional
<><>
Draining abscesses → environmental contamination
◦ Can be of benefit to individual
◦ Local treatment – flush abscess cavity w dilute iodine or chlorhexidine

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12
Q

Caseous Lymphadenitis
Prevention:

A

Avoid introduction of an infected animal into the flock.
◦ This relies on a test that correctly identifies the animals.
◦ With reliability issues in the test, repeated testing and staged introduction would be one
method.
<><>
Vaccination: vaccines could protect a clean flock, but are not yet sufficiently reliable
<><>
Control:
◦ Eradication: identification and removal of infected animals.

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13
Q

Caseous Lymphadenitis
Vaccination:
- efficacy?

A

◦ Reduces severity of signs in endemic flocks
◦ Reduces economic loss
◦ Cannot use to eradicate the disease
◦ Number of vaccines available

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14
Q

Bovine Leukosis - other names?

A

Enzootic Leukosis
Sporadic Leukosis
etc….

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15
Q

Enzootic Bovine Leukosis
- type of disease
- etiology
- tissues affected
- result

A
  • Neoplastic disease
  • Induced by a retrovirus: BLV
  • Almost any tissue affected
  • Highly fatal once clinical
  • Viral infection ≠ lymphoma
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16
Q

Enzootic Bovine Leukosis
- pathogen

A

Etiology: BLV – oncogenic type-C virus
- retroviridae
- enveloped virus

17
Q

Enzootic Bovine Leukosis
- infects what cells?
- antibodies?
- detection of infection?
- duration?

A
  • Virus persists mainly in B-lymphocytes
    ◦ Also monocytes, macrophages in pro-viral cell-associated, non-active form
  • Antibodies produced but non-protective
  • Seropositivity reliably indicates infection > In animals over 6 months
  • Infection considered permanent
18
Q

Enzootic Bovine Leukosis
- epidemiology: who gets it? pattern?

A

Epidemiology: (clinical disease)
* not well understood
<><>
* Herd size and infection rate (positive correlation?)
* Higher rate dairy herds > Herd size, age, genetics?
* Higher rate certain families (BoLA-type) > Predisposition through antigens of Major Histocompatibility Complex (MHC)
*No seasonal pattern for clinical lymphosarcoma

19
Q

Enzootic Bovine Leukosis
Factors influencing clinical disease

A

◦ Age
◦ Level of infection in herd
◦ Opportunities for contact
◦ Status of dam
◦ Inter-current disease/stress
◦ Genetic factors

20
Q

Enzootic Bovine Leukosis
Transmission:

A

Horizontal (primary mode: ≈18 months)
◦ True natural transmission - Cow-to-cow spread
◦ Transmission by blood-contaminated equipment
> Blood collection, tattooing, ear tags, dehorning, rectal palpation
> AI – passage from semen of infected bulls not shown
<><><><>
Vertical (less likely)
◦ Maternal antibodies in milk may be protective
◦ In utero or during calving (4-10% of positive cases)

21
Q

Enzootic Bovine Leukosis
Disease prevalence? what diseases?

A

◦ Seropositive: Variable numbers reported
> Farm level high (as many as 80% positive)
> 5-40% cattle reported as positive
> Prevalence increased after 24 months-of-age
<><><><>
Clinically affected:
◦ Persistent Lymphocytosis (PL): approx 30% of seropositive animals
◦ Lymphoma: 1-5% of seropositive animals

22
Q

Enzootic Bovine Leukosis
- what determines if an animal will express disease?

A

◦ Influenced by genetic susceptibility
◦ Explains why so few animals have clinical disease
◦ Explains why slow disease spread
<><><><>
Variability animal to animal
◦ Multifactorial effect on expression of disease

23
Q

Enzootic Bovine Leukosis
- as a retrovirus, what does it rely on the host for?

A

◦ Latency, relies on cell for replication, cell transformation

24
Q

Enzootic Bovine Leukosis
- affects what cells, mostly?
- two main disease presentations?

A

B-Cells
<><><><>
Persistent lymphocytosis (count variable, up to 100 x109/L)
◦ Subclinical lymphoproliferative state
◦ ?pre-lymphosarcoma?
◦ Expression of tumor-associated antigen on circulating lymphocytes
<><><><>
Multicentric lymphosarcoma
◦ Adults >2 years of age
◦ Most 4-8 years
◦ Sporadic in herd

25
Q

Enzootic Bovine Leukosis
Multi-centric lymphosarcoma
- clinical signs

A

◦ Variable: depends on organs affected
◦ General: weight loss, reduced production
<><>
Frequent target organs:
◦ Lymph node enlargement: external or internal
◦ Thoracic LN: obstruction to venous drainage
◦ Retrobulbar masses may cause exophthalmus
◦ Abomasal wall: diarrhea, melena, outflow obstruction
◦ Myocardium (right atrium): congestive heart failure, arrhythmias
◦ Renal, uterus, skeletal muscle, retropharyngeal LN
◦ Meninges, posterior paralysis

26
Q

Enzootic Bovine Leukosis
- Dx for persistent lymphocytosis and multicentric lymphosarcoma diseases

A

Persistent lymphocytosis
◦ CBC: cell counts, ratios >25% immature cells, morphology
◦ False positives common
<><><><>
Multicentric lymphosarcoma
◦ Any adult with lymphadenopathy
◦ LN aspirate (not reliable), ddx reactive lymph node
◦ CBC not rewarding
◦ Serology and post-mortem

27
Q

Enzootic Bovine Leukosis
Testing

A

◦ ELISA – more sensitive than traditional AGID
<><>
◦ PCR very reliable, nested PCR
> Useful in eradication programs
> Expensive
<><>
◦ Combined ELISA/PCR
<><>
◦ Loop-mediated isothermal amplification (LAMP) assay
> As sensitive as single PCR, do not need a thermocycler

28
Q

Enzootic Bovine Leukosis
◦ Agar gel immunodiffusion (AGID) method for testing, pros and cons?

A

◦ Sensitivity 99.8%, specificity 98.5%
<><>
False negatives
◦ Some animals do not develop high levels of AB
◦ AB not detectible for up to 20 days post-infection
◦ Post-calving sequestration - mammary gland
<><>
False positives
◦ First 2-7 months after birth from positive dam
◦ Post blood/plasma transfusion

29
Q

Enzootic Bovine Leukosis
Control

A
  • some countries attempting eradication
  • already eradicated in a number of EU countries
  • no vaccines
30
Q

Sporadic Bovine Leukosis
- what is this?
- cells affected?

A

Group of neoplastic diseases of the lymphatic tissue not associated with
BLV:
1. Juvenile multi-centric lymphoma
2. Thymic lymphoma
3. Cutaneous lymphoma
4. Atypical Forms
<><>
B- or T-cell lineage

31
Q

Sporadic Bovine Leukosis
> Juvenile lymphoma
- age affected, prevalence
- disease course
- clinical signs
- pathogenesis

A

◦ Age: 3 - 6 months-of-age (range 1-month to 3-years-of age)
◦ Prevalence unknown, considered rare
◦ Rapid course - weeks, often sudden onset
◦ Clinical signs:
◦ Weight loss, depression, anemia, lymphadenopathy, variable signs depending on organ involvement (lymph nodes, liver, kidney, spleen, uterus, heart, spinal column
nodes)
◦ Bone marrow infiltration → anemia, leukemia
◦ BLV independent (ie. not virus-associated)

32
Q

Sporadic Bovine Leukosis
> Cutaneous lymphoma
- age
- lesions, locations
- progression

A

◦ Age: 1-3 years-of-age
◦ Dermal lesions
◦ Usually dorsum, hind limbs, perineal areas
◦ May progress to multicentric (may have organ involvement)
◦ Lesions: 3 cm, necrotic centers, May regress and recur

33
Q

Sporadic Bovine Leukosis
> Thymic lymphoma
- prevalence
- breeds
- age
- signs

A

◦ Rare
◦ Beef breeds more common
◦ Age: 6 months - 2 years (range: newborn to 4-years-old)
◦ Signs associated with mass in mediastinum > Obstruction of venous return from front end
◦ Jugular distension, edema, may have thoracic fluid > Interference with respiration, eructation (bloat)

34
Q

Sporadic Bovine Leukosis
> Atypical Forms
- what are these? what can they affect?

A

(individual cases in the literature)
◦ Muscle
◦ Trachea, skin
<><>
Alpaca:
◦ Mandibular masses, weight loss
◦ Disseminated small lymphoma – pancreas, kidney, liver, omentum, caudal vena cava
◦ BLV proviral DNA detect in some tissues

35
Q

Bovine Immunodeficiency
Virus
- pathogen?
- similar to?
- disease?
- associations?

A

◦ Family – Retroviridae
◦ Genus - Lentivirus
◦ BIV - similar to human, simian, feline immunodeficiency viruses.
Also EIA
◦ Does not appear to cause clinical disease
◦ May be associated with lymphadenopathy, lymphocytosis, decreased milk
production, CNS disease, weakness.

36
Q

Bovine Immunodeficiency
Virus
- prevalence?
- production parameters?
- management?

A

◦ Prevalence low but not uncommon
◦ May be associated with decreased milk production
◦ Management – decrease cattle contact may decrease spread

3. Food Animal 3 (23 decks)

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